PPARγ ligands decrease hydrostatic pressure-induced platelet aggregation and proinflammatory activity.

Hypertension is known to be associated with platelet overactivity, but the direct effects of hydrostatic pressure on platelet function remain unclear. The present study sought to investigate whether elevated hydrostatic pressure is responsible for platelet activation and to address the potential role of peroxisome proliferator-activated receptor-γ (PPARγ). We observed that hypertensive patients had significantly higher platelet volume and rate of ADP-induced platelets aggregation compared to the controls.

The involvement of the CD40-CD40L pathway in activated platelet-induced changes in HUVEC COX-2 and PPARα expression.

We aim to determine the extent of the CD40-CD40L pathway involvement in activated platelet-induced changes in human umbilical endothelial cells (HUVECs). Activated platelets were co-incubated with HUVECs in the presence or absence of CD40LmAb. HUVECs were also directly stimulated with rhCD40L.